We have found that young patients with essential hypertension have defective modulation of the brachial arterial dicrotic wave. A circulatory model which we developed explains the abnormality in terms of increased arterial rigidity and decreased vasodilator responsiveness. The magnitude of the defect was related to sympathetic neural activity as reflected by arterial plasma concentrations of norepinephrine (NE), the sympathetic neurotransmitter. Using arterial pulse wave velocity and forearm plethysmography to indicate brachial arterial stiffness and mean arteriolar caliber, we plan to determine the separate contributions of arterial rigidity and vasodilatory failure to the vascular abnormalities which occur early in the development of essential hypertension. Pilot results suggest the possibility that arterial stiffness -- true arteriosclerosis -- may cause overestimation of intra-arterial pressure based on measurements by cuff, and this stiffness may have a neurogenic component.